Relevant bibliographies by topics / My3D

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Academic literature on the topic 'My3D'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "My3D"

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Patapoutian, A., J. K. Yoon, J. H. Miner, S. Wang, K. Stark, and B. Wold. "Disruption of the mouse MRF4 gene identifies multiple waves of myogenesis in the myotome." Development 121, no. 10 (October 1, 1995): 3347–58. http://dx.doi.org/10.1242/dev.121.10.3347.

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MRF4 (herculin/Myf-6) is one of the four member MyoD family of transcription factors identified by their ability to enforce skeletal muscle differentiation upon a wide variety of nonmuscle cell types. In this study the mouse germline MRF4 gene was disrupted by targeted recombination. Animals homozygous for the MRF4bh1 allele, a deletion of the functionally essential bHLH domain, displayed defective axial myogenesis and rib pattern formation, and they died at birth. Differences in somitogenesis between homozygous MRF4bh1 embryos and their wild-type littermates provided evidence for three distinct myogenic regulatory programs (My1-My3) in the somite, which correlate temporally and spatially with three waves of cellular recruitment to the expanding myotome. The first program (My1), marked initially by Myf-5 expression and followed by myogenin, began on schedule in the MRF4bh1/bh1 embryos at day 8 post coitum (E8). A second program (My2) was highly deficient in homozygous mutant MRF4 embryos, and normal expansion of the myotome failed. Moreover, expression of downstream muscle-specific genes, including FGF-6, which is a candidate regulator of inductive interactions, did not occur normally. The onset of MyoD expression around E10.5 in wild-type embryos marks a third myotomal program (My3), the execution of which was somewhat delayed in MRF4 mutant embryos but ultimately led to extensive myogenesis in the trunk. By E15 it appeared to have largely compensated for the defective My2 program in MRF4 mutants. Homozygous MRF4bh1 animals also showed improper rib pattern formation perhaps due to the absence of signals from cells expressing the My2 program. Finally, a later and relatively mild phenotype was detected in intercostal muscles of newborn animals.
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Maleki, Soheila J., Catherine A. Royer, and Barry K. Hurlburt. "MyoD−E12 Heterodimers and MyoD−MyoD Homodimers Are Equally Stable†." Biochemistry 36, no. 22 (June 1997): 6762–67. http://dx.doi.org/10.1021/bi970262m.

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Song, An, Qi Wang, Mark G. Goebl, and Maureen A. Harrington. "Phosphorylation of Nuclear MyoD Is Required for Its Rapid Degradation." Molecular and Cellular Biology 18, no. 9 (September 1, 1998): 4994–99. http://dx.doi.org/10.1128/mcb.18.9.4994.

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ABSTRACT MyoD is a basic helix-loop-helix transcription factor involved in the activation of genes encoding skeletal muscle-specific proteins. Independent of its ability to transactivate muscle-specific genes, MyoD can also act as a cell cycle inhibitor. MyoD activity is regulated by transcriptional and posttranscriptional mechanisms. While MyoD can be found phosphorylated, the functional significance of this posttranslation modification has not been established. MyoD contains several consensus cyclin-dependent kinase (CDK) phosphorylation sites. In these studies, we examined whether a link could be established between MyoD activity and phosphorylation at putative CDK sites. Site-directed mutagenesis of potential CDK phosphorylation sites in MyoD revealed that S200 is required for MyoD hyperphosphorylation as well as the normally short half-life of the MyoD protein. Additionally, we determined that turnover of the MyoD protein requires the proteasome and Cdc34 ubiquitin-conjugating enzyme activity. Results of these studies demonstrate that hyperphosphorylated MyoD is targeted for rapid degradation by the ubiquitin pathway. The targeted degradation of MyoD following CDK phosphorylation identifies a mechanism through which MyoD activity can be regulated coordinately with the cell cycle machinery (CDK2 and CDK4) and/or coordinately with the cellular transcriptional machinery (CDK7, CDK8, and CDK9).
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Kitzmann, Magali, Marie Vandromme, Valerie Schaeffer, Gilles Carnac, Jean-Claude Labbé, Ned Lamb, and Anne Fernandez. "cdk1- and cdk2-Mediated Phosphorylation of MyoD Ser200 in Growing C2 Myoblasts: Role in Modulating MyoD Half-Life and Myogenic Activity." Molecular and Cellular Biology 19, no. 4 (April 1, 1999): 3167–76. http://dx.doi.org/10.1128/mcb.19.4.3167.

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ABSTRACT We have examined the role of protein phosphorylation in the modulation of the key muscle-specific transcription factor MyoD. We show that MyoD is highly phosphorylated in growing myoblasts and undergoes substantial dephosphorylation during differentiation. MyoD can be efficiently phosphorylated in vitro by either purified cdk1-cyclin B or cdk1 and cdk2 immunoprecipitated from proliferative myoblasts. Comparative two-dimensional tryptic phosphopeptide mapping combined with site-directed mutagenesis revealed that cdk1 and cdk2 phosphorylate MyoD on serine 200 in proliferative myoblasts. In addition, when the seven proline-directed sites in MyoD were individually mutated, only substitution of serine 200 to a nonphosphorylatable alanine (MyoD-Ala200) abolished the slower-migrating hyperphosphorylated form of MyoD, seen either in vitro after phosphorylation by cdk1-cyclin B or in vivo following overexpression in 10T1/2 cells. The MyoD-Ala200 mutant displayed activity threefold higher than that of wild-type MyoD in transactivation of an E-box-dependent reporter gene and promoted markedly enhanced myogenic conversion and fusion of 10T1/2 fibroblasts into muscle cells. In addition, the half-life of MyoD-Ala200 protein was longer than that of wild-type MyoD, substantiating a role of Ser200 phosphorylation in regulating MyoD turnover in proliferative myoblasts. Taken together, our data show that direct phosphorylation of MyoD Ser200 by cdk1 and cdk2 plays an integral role in compromising MyoD activity during myoblast proliferation.
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Tintignac, Lionel A. J., Valentina Sirri, Marie Pierre Leibovitch, Yann Lécluse, Maria Castedo, Didier Metivier, Guido Kroemer, and Serge A. Leibovitch. "Mutant MyoD Lacking Cdc2 Phosphorylation Sites Delays M-Phase Entry." Molecular and Cellular Biology 24, no. 4 (February 15, 2004): 1809–21. http://dx.doi.org/10.1128/mcb.24.4.1809-1821.2004.

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ABSTRACT The transcription factors MyoD and Myf-5 control myoblast identity and differentiation. MyoD and Myf-5 manifest opposite cell cycle-specific expression patterns. Here, we provide evidence that MyoD plays a pivotal role at the G2/M transition by controlling the expression of p21Waf1/Cip1 (p21), which is believed to regulate cyclin B-Cdc2 kinase activity in G2. In growing myoblasts, MyoD reaccumulates during G2 concomitantly with p21 before entry into mitosis; MyoD is phosphorylated on Ser5 and Ser200 by cyclin B-Cdc2, resulting in a decrease of its stability and down-regulation of both MyoD and p21. Inducible expression of a nonphosphorylable MyoD A5/A200 enhances the MyoD interaction with the coactivator P/CAF, thereby stimulating the transcriptional activation of a luciferase reporter gene placed under the control of the p21 promoter. MyoD A5/A200 causes sustained p21 expression, which inhibits cyclin B-Cdc2 kinase activity in G2 and delays M-phase entry. This G2 arrest is not observed in p21−/− cells. These results show that in cycling cells MyoD functions as a transcriptional activator of p21 and that MyoD phosphorylation is required for G2/M transition.
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Montarras, D., F. Aurade, T. Johnson, J. IIan, F. Gros, and C. Pinset. "Autonomous differentiation in the mouse myogenic cell line, C2, involves a mutual positive control between insulin-like growth factor II and MyoD, operating as early as at the myoblast stage." Journal of Cell Science 109, no. 3 (March 1, 1996): 551–60. http://dx.doi.org/10.1242/jcs.109.3.551.

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We have studied the contribution of the endogenous production of insulin-like growth factor II (IGFII) and of the muscle regulatory factor, MyoD, to the autonomy of differentiation in isolated skeletal myoblasts. Inhibition of MyoD and IGFII gene expression in myoblasts of the mouse myogenic cell line, C2, was achieved by transfection and selection of stably transfected cells (anti-MyoD and anti-IGFII cells) with vectors producing MyoD or IGFII antisense RNA. We observed that inhibiting either MyoD or IGFII has multiple and similar consequences. In addition to the inhibition of the target gene, expression of MyoD transcripts in anti-IGFII myoblasts and expression of IGFII in anti-MyoD myoblasts were also abolished, whereas accumulation of transcripts for the muscle regulatory factor, Myf5, was markedly increased in both cell types. However, despite this Myf5 up-regulation, both anti-IGFII and anti-MyoD myoblasts lost the ability to undergo autonomous differentiation (differentiation in the absence of added IGF), further indicating that Myf5 and MyoD are not strictly interchangeable. Additional evidence of a link between MyoD and IGFII was obtained: (1) forced expression of the MyoD cDNA stimulated IGFII gene expression, and (2) treatment of C2 myoblasts with fibroblast growth factor, not only diminished MyoD expression and compromised differentiation as previously shown by others, but also abolished IGFII expression. These experiments showing loss or gain of function argue in favor of a mutual positive control between IGFII and MyoD operating as early as the myoblast stage.
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Thorburn, A. M., P. A. Walton, and J. R. Feramisco. "MyoD induced cell cycle arrest is associated with increased nuclear affinity of the Rb protein." Molecular Biology of the Cell 4, no. 7 (July 1993): 705–13. http://dx.doi.org/10.1091/mbc.4.7.705.

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In studying the mechanism through which the myogenic determination protein MyoD prevents entry into the S phase of the cell cycle, we have found a relationship between MyoD and the retinoblastoma (Rb) tumor suppressor protein. By direct needle microinjection of purified recombinant MyoD protein into quiescent fibroblasts, which were then induced to proliferate by serum, we found that MyoD arrested progression of the cell cycle, in agreement with studies utilizing expression constructs for MyoD. By studying temporal changes in cells injected with MyoD protein, it was found that MyoD did not prevent serum induced expression of the protooncogene c-Fos, an event that occurs in the G0 to G1 transition of the cycle. Injection of the MyoD protein as late as 8 h after the addition of serum still caused an inhibition in DNA synthesis, suggesting that MyoD inhibits the G1 to S transition as opposed to the G0 to G1 transition. MyoD injection did not prevent the expression of cyclin A. However MyoD injection did result in a block in the increase in Rb extractibility normally seen in late G1 phase cells. As this phenomenon is associated with the hyperphosphorylation of Rb at this point in the cell cycle and is correlated with progression into S phase, this provides further evidence that MyoD blocks the cycle late in G1.
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Staib, Jessica L., Steven J. Swoap, and Scott K. Powers. "Diaphragm contractile dysfunction in MyoD gene-inactivated mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 3 (September 1, 2002): R583—R590. http://dx.doi.org/10.1152/ajpregu.00080.2002.

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MyoD is one of four myogenic regulatory factors found exclusively in skeletal muscle. In an effort to better understand the role that MyoD plays in determining muscle contractile properties, we examined the effects of MyoD deletion on both diaphragmatic contractile properties and myosin heavy chain (MHC) phenotype. Regions of the costal diaphragm from wild-type and MyoD knockout [ MyoD (−/−)] adult male BALB/c mice ( n = 8/group) were removed, and in vitro diaphragmatic contractile properties were measured. Diaphragmatic contractile measurements revealed that MyoD (−/−) animals exhibited a significant ( P < 0.05) downward shift in the force-frequency relationship, a decrement in maximal specific tension (Po; −33%), a decline in maximal shortening velocity (Vmax; −37%), and concomitant decrease in peak power output (−47%). Determination of MHC isoforms in the diaphragm via gel electrophoresis revealed that MyoD elimination resulted in a fast-to-slow shift ( P < 0.05) in the MHC phenotype toward MHC types IIA and IIX in MyoD (−/−) animals. These data indicate that MyoD deletion results in a decrease in diaphragmatic submaximal force generation and Po, along with decrements in both Vmax and peak power output. Hence, MyoD plays an important role in determining diaphragmatic contractile properties.
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Reynaud, Emmanuel G., Karine Pelpel, Martine Guillier, Marie Pierre Leibovitch, and Serge A. Leibovitch. "p57Kip2 Stabilizes the MyoD Protein by Inhibiting Cyclin E-Cdk2 Kinase Activity in Growing Myoblasts." Molecular and Cellular Biology 19, no. 11 (November 1, 1999): 7621–29. http://dx.doi.org/10.1128/mcb.19.11.7621.

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ABSTRACT We show that expression of p57Kip2, a potent tight-binding inhibitor of several G1cyclin–cyclin-dependent kinase (Cdk) complexes, increases markedly during C2C12 myoblast differentiation. We examined the effect of p57Kip2 on the activity of the transcription factor MyoD. In transient transfection assays, transcriptional transactivation of the mouse muscle creatine kinase promoter by MyoD was enhanced by the Cdk inhibitors. In addition, p57Kip2, p21Cip1, and p27Kip1 but not p16Ink4a induced an increased level of MyoD protein, and we show that MyoD, an unstable nuclear protein, was stabilized by p57Kip2. Forced expression of p57Kip2 correlated with hypophosphorylation of MyoD in C2C12 myoblasts. A dominant-negative Cdk2 mutant arrested cells at the G1 phase transition and induced hypophosphorylation of MyoD. Furthermore, phosphorylation of MyoD by purified cyclin E-Cdk2 complexes was inhibited by p57Kip2. In addition, the NH2 domain of p57Kip2 necessary for inhibition of cyclin E-Cdk2 activity was sufficient to inhibit MyoD phosphorylation and to stabilize it, leading to its accumulation in proliferative myoblasts. Taken together, our data suggest that repression of cyclin E-Cdk2-mediated phosphorylation of MyoD by p57Kip2 could play an important role in the accumulation of MyoD at the onset of myoblast differentiation.
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Goldhamer, D. J., B. P. Brunk, A. Faerman, A. King, M. Shani, and C. P. Emerson. "Embryonic activation of the myoD gene is regulated by a highly conserved distal control element." Development 121, no. 3 (March 1, 1995): 637–49. http://dx.doi.org/10.1242/dev.121.3.637.

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MyoD belongs to a small family of basic helix-loop-helix transcription factors implicated in skeletal muscle lineage determination and differentiation. Previously, we identified a transcriptional enhancer that regulates the embryonic expression of the human myoD gene. This enhancer had been localized to a 4 kb fragment located 18 to 22 kb upstream of the myoD transcriptional start site. We now present a molecular characterization of this enhancer. Transgenic and transfection analyses localize the myoD enhancer to a core sequence of 258 bp. In transgenic mice, this enhancer directs expression of a lacZ reporter gene to skeletal muscle compartments in a spatiotemporal pattern indistinguishable from the normal myoD expression domain, and distinct from expression patterns reported for the other myogenic factors. In contrast to the myoD promoter, the myoD enhancer shows striking conservation between humans and mice both in its sequence and its distal position. Furthermore, a myoD enhancer/heterologous promoter construct exhibits muscle-specific expression in transgenic mice, demonstrating that the myoD promoter is dispensable for myoD activation. With the exception of E-boxes, the myoD enhancer has no apparent sequence similarity with regulatory regions of other characterized muscle-specific structural or regulatory genes. Mutation of these E-boxes, however, does not affect the pattern of lacZ transgene expression, suggesting that myoD activation in the embryo is E-box-independent. DNase I protection assays reveal multiple nuclear protein binding sites in the core enhancer, although none are strictly muscle-specific. Interestingly, extracts from myoblasts and 10T1/2 fibroblasts yield identical protection profiles, indicating a similar complement of enhancer-binding factors in muscle and this non-muscle cell type. However, a clear difference exists between myoblasts and 10T1/2 cells (and other non-muscle cell types) in the chromatin structure of the chromosomal myoD core enhancer, suggesting that the myoD enhancer is repressed by epigenetic mechanisms in 10T1/2 cells. These data indicate that myoD activation is regulated at multiple levels by mechanisms that are distinct from those controlling other characterized muscle-specific genes.
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Dissertations / Theses on the topic "My3D"

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Souza, Alyson Matheus de Carvalho. "Investigando a compress?o da percep??o de dist?ncia em ambientes virtuais atrav?s da compara??o entre dispositivos de visualiza??o." Universidade Federal do Rio Grande do Norte, 2014. http://repositorio.ufrn.br/handle/123456789/19664.

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A percep??o correta de dist?ncias ? importante para a execu??o de diversas tarefas interativas, como navega??o, sele??o e manipula??o. ? sabido, no entanto, que, em geral, existe uma significativa compress?o das dist?ncias percebidas em ambientes virtuais, principalmente quando h? a utiliza??o de Head-Mounted Displays - HMDs. Essa compress?o de dist?ncias percebidas pode trazer ? aplica??o diversos problemas e at? afetar negativamente a utilidade de aplica??es que dependem desse julgamento correto. A comunidade cient?fica, at? o presente, n?o conseguiu determinar as causas do fen?meno da compress?o da percep??o de dist?ncia em ambientes virtuais. Por esse motivo, foi o objetivo desse trabalho buscar, atrav?s de experimentos com usu?rios, encontrar pistas sobre a influ?ncia do field-of-view - FoV - e dos m?todos para estimativas de dist?ncias nessa compress?o percebida. Para tal, foi feita uma compara??o experimental entre o my3D e o HMD, utilizando 32 participantes, a fim de encontrar pistas sobre as causas da percep??o comprimida. Os resultados indicaram que o my3D possui capacidades inferiores ao HMD, produzindo estimativas piores, em m?dia, em ambos os m?todos de estimativa testados. As causas apontadas para tal foram o est?mulo incorreto da vis?o perif?rica, o FoV inferior e a menor imers?o, segundo descrito pelos participantes do experimento
The correct distance perception is important for executing various interactive tasks such as navigation, selection and manipulation. It is known, however, that, in general, there is a significant distance perception compression in virtual environments, mainly when using Head-Mounted Displays - HMDs. This perceived distance compression may bring various problems to the applications and even affect in a negative way the utility of those applications that depends on the correct judgment of distances. The scientific community, so far, have not been able to determine the causes of the distance perception compression in virtual environments. For this reason, it was the objective of this work to investigate, through experiments with users, the influence of both the field-of-view - FoV - and the distance estimation methods on this perceived compression. For that, an experimental comparison between the my3D device and a HMD, using 32 participants, seeking to find information on the causes of the compressed perception, was executed. The results showed that the my3D has inferior capabilities when compared to the HMD, resulting in worst estimations, on average, in both the tested estimation methods. The causes of that are believed to be the incorrect stimulus of the peripheral vision of the user, the smaller FoV and the smaller immersion sense, as described by the participants of the experiment.
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Xiao, Lei. "Transcriptional Regulation of the Xenopus MyoD Gene." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-11960.

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Brunelli, Roberta de Matos 1985. "Os efeitos do laser de baixa potência no processo de reparo muscular após criolesão em ratos = The effects of low-level laser therapy on muscle healing process after cryolesion." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308777.

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Orientadores: Daniela Cristina Carvalho de Abreu, Alberto Cliquet Junior
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O objetivo deste estudo foi verificar os efeitos da laserterapia de baixa potência no comprimento de onda ?=780nm entre diferentes períodos de tratamento 7, 14 e 21 dias e verificar a dose (10J/cm2 ou 50J/cm2) que promove melhor reparo muscular através das análises histopatológicas e imunohistoquímicas. Foram utilizados 54 ratos machos divididos em 3 grupos: GC: grupo controle (criolesão, sem tratamento); G10: criolesão do músculo tibial anterior (TA) e tratados com laser dose 10J/cm² e G50: criolesão do músculo TA e tratados com laser dose 50J/cm² que foram subdivididos em 3 subgrupos (n=6): 7, 14 e 21 dias de tratamento. Os achados histopatológicos revelaram maior organização das fibras musculares dos grupos tratados com laser 10J/cm² e 50J/cm² durante os períodos 7 e 14 dias em relação ao grupo controle; no período 21 dias os grupos apresentaram semelhanças na reparação tecidual. Em relação à área da lesão os grupos tratados com laser 10J/cm² e 50J/cm² durante 7 dias obtiveram diminuição significativa (p ? 0.05) da área da lesão em relação ao grupo controle, sendo que os grupos 14 e 21 dias não apresentaram diferenças significativas entre eles. Na contagem dos vasos o grupo tratado com laser 10J/cm² no 14° dia apresentou aumento dos vasos em relação ao grupo tratado com dose 50J/cm², mas não em relação ao grupo controle. Nos tempos de 7 e 21 dias os grupos não apresentaram diferença significativa entre si. Com relação às análises imunohistoquímicas da myoD no período de 7 dias os grupos tratados com laser 10J/cm² e 50J/cm² apresentaram maior imunomarcação comparada com o grupo controle, no período 14 e 21 dias a imunomarcação estava ausente. A imunomarcação da miogenina estava presente de forma semelhante nos períodos 7 e 14 dias para os três grupos analisados e no período 21 dias a imunomarcação da miogenina estava ausente em todos os grupos experimentais. Os resultados mostraram que o laser possui efeitos positivos no reparo muscular
Abstract: The objective of this study was to assess the effects of 780nm low-level laser therapy at different periods of 7, 14 and 21 days after cryolesion, including the dose (10 or 50J/cm2) to promote a better muscle repair evidenced by histopathological and immumohistochemical analyses. Fifty-four male rats were divided into three groups: injured control group (CG) - injured animals without any treatment; injured 780nm laser treated group, at 10 J/cm² (G10) and injured 780nm laser treated group, at 50 J/cm² (G50). Each group was divided into 3 subgroups (n=6): 7, 14 and 21 days post-injury. Histopathological findings revealed better-organized muscle fibers in the G10 and G50 during the periods of 7 and 14 days compared to CG. The G10 and G50 during 7 days showed a significant reduction (p? 0.05) of lesion area compared to CG, without differences between groups treated for 14 and 21 days. The G10 showed an increase of the amount of vessels after 14 days compared to the G50, but not in relation to controls. With regard to the immumohistochemical analyses of the MyoD factor, The G10 and G50 during 7 days showed higher concentrations of immunomarkers than controls. Myogenin immunomarkers were similarly observed at days 7 and 14 in all three groups analyzed, whereas immunomarkers were found in none of the groups after 21 days of laser therapy. The results showed that laser has positive effects on muscle repair
Mestrado
Fisiopatologia Cirúrgica
Mestra em Ciências
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Armour, Christine. "Regulation of MyoD induced myogenesis in P19 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq26299.pdf.

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Maguire, Richard John. "Identifying targets of MyoD in myogenic stem cells." Thesis, University of York, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516609.

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Musgrove, Nicholas James. "Land use and vegetation change on the Long Mynd." Thesis, University of Wolverhampton, 2009. http://hdl.handle.net/2436/84479.

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The plant communities of the Long Mynd plateau are the culmination of over 3000 years of human intervention that largely deforested the uplands, and subsequently maintained the generally treeless heath and grassland communities now extant. The capacity of these communities to respond to directional change is well known, indeed the traditional mode of heathland management, burning, depends on the regenerative capacity of the target species, generally heather (Calluna vulgaris), for its success. However, changes in post WW2 stocking practice; the loss of ponies followed by an increase in the numbers of sheep and a change to them being overwintered on the hill, led to excessive grazing and damage to the heath. This coincided with the spread over the hill by bracken (Pteridium aquilinum) and other changes in the distribution and nature of the vegetation. A sequence of vegetation surveys made by various individuals and organisations over the past 75 years or so has been analysed in an attempt to delineate spatial and temporal changes in the vegetation. This demonstrated the need for a standardised survey methodology to allow consistent monitoring. The analysis showed that bracken had been infiltrating most of the communities from its origins outside the lower limits of the Common as well as from some of the valley sides. Within the last decade, this expansion has apparently been contained in line with the current management plan for control. A survey of 730 quadrats in some 30 stands was made to characterise the variation of the vegetation on the plateau, and to relate it to some of the associated environmental factors. Classification, unconstrained ordination and ordination constrained by the abiotic environmental variables, showed that, a) the strongest trend in the vegetation distinguished water-flushed communities, b) non-wetland communities differentiate between heathland and grassland, c) this trend can be only partly be attributed to the measured abiotic environmental variables, d) the amount of pure Pteridietum [U20] is limited, although much of the heathland and grassland has bracken within it. There are indications that invasion by bracken often correlates with a loss of dominance of Calluna in favour of Deschampsia flexuosa and Vaccinium myrtillus. Difficulties in associating these trends with measured abiotic variables suggests, other factors probably management processes, are critical in driving this trend. Distribution of ‘heathland’ bryophytes was found to be associated more with the structure of their ‘host’ vascular communities rather than with abiotic factors. Finally, this investigation considers the practical implications with regard to the future encouragement of heather and the control of bracken. Cutting rather than burning appears to be the ecologically most suitable method for heather regeneration and bracken control.
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Thompson, Elizabeth Claire. "Studies on SET and MYND domain proteins in Drosophila." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612456.

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Wang, Jianyu. "Effects of mechanical overload and aging on MyoD and effects of oxandrolone treatment and overload on IGF-1 and MyoD in old rats /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488186329501203.

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Scionti, Isabella. "Epigenetic Regulation of Skeletal Muscle Differentiation." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN084/document.

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LSD1 et PHF2 sont des déméthylases de lysines capables de déméthyler à la fois les protéines histones qui influencent l’expression génique et les protéines non histones en affectant leurs activités ou stabilités. Des approches fonctionnelles d’inactivation de Lsd1 ou Phf2 chez la souris ont démontré l’implication de ces enzymes dans l'engagement des cellules progénitrices au cours de la différenciation. La myogenèse est l'un des exemples les mieux caractérisés sur la façon dont les cellules progénitrices se multiplient et se différencient pour former un organe fonctionnel. Elle est initiée par une expression temporelle spécifique des gènes régulateurs cibles. Parmi ces facteurs, MYOD est un régulateur clé de l'engagement dans la différenciation des cellules progénitrices musculaires. Bien que l’action de MYOD au cours de la différenciation cellulaire ait été largement étudiée, peu de chose sont connus sur les événements de remodelage de la chromatine associés à l'activation de l'expression de MyoD. Parmi les régions régulatrices de l'expression de MyoD, la région Core Enhancer (CE) qui est transcrite en ARN activateur non codant (CEeRNA) a été démontrée pour contrôler l'initiation de l'expression de MyoD au cours de l'engagement de myoblastes dans la différenciation.Nous avons identifié LSD1 et PHF2 comme des activateurs clés du CE de MyoD. L'invalidation in vitro et in vivo de LSD1 ou l'inhibition de l'activité enzymatique de LSD1 empêche le recrutement de l'ARN PolII sur le CE, empêchant l’expression du CEeRNA. D’après nos résultats, l'expression forcée du CEeRNA restaure efficacement l'expression de MyoD et la fusion myoblastique en l'absence de LSD1. De plus, PHF2 interagit avec LSD1 en régulant sa stabilité protéique.En effet, l'ablation in vitro de PHF2 entraîne une dégradation massive de LSD1 et donc une absence d'expression du CEeRNA. Cependant, toutes les modifications d'histones qui ont lieu dans la région du CE lors de l'activation de la différenciation ne peuvent pas être directement attribuées à l'activité enzymatique de LSD1 ou PHF2. Ces résultats soulèvent la question de l'identité des partenaires de LSD1 et PHF2, qui co-participeraient à l'expression du CEeRNA et donc à l'engagement des myoblastes dans la différenciation cellulaire
LSD1 and PHF2 are lysine de-methylases that can de-methylate both histone proteins, influencing gene expression and non-histone proteins, affecting their activity or stability. Functional approaches using Lsd1 or Phf2 inactivation in mouse have demonstrated the involvement of these enzymes in the engagement of progenitor cells into differentiation. One of the best-characterized examples of how progenitor cells multiply and differentiate to form functional organ is myogenesis. It is initiated by the specific timing expression of the specific regulatory genes; among these factors, MYOD is a key regulator of the engagement into differentiation of muscle progenitor cells. Although the action of MYOD during muscle differentiation has been extensively studied, still little is known about the chromatin remodeling events associated with the activation of MyoD expression. Among the regulatory regions of MyoD expression, the Core Enhancer region (CE), which transcribes for a non-coding enhancer RNA (CEeRNA), has been demonstrated to control the initiation of MyoD expression during myoblast commitment. We identified LSD1 and PHF2 as key activators of the MyoD CE. In vitro and in vivo ablation of LSD1 or inhibition of LSD1 enzymatic activity impaired the recruitment of RNA PolII on the CE, resulting in a failed expression of the CEeRNA. According to our results, forced expression of the CEeRNA efficiently rescue MyoD expression and myoblast fusion in the absence of LSD1. Moreover PHF2 interacts with LSD1 regulating its protein stability. Indeed in vitro ablation of PHF2 results in a massive LSD1 degradation and thus absence of CEeRNA expression. However, all the histone modifications occurring on the CE region upon activation cannot be directly attributed to LSD1 or PHF2 enzymatic activity. These results raise the question of the identity of LSD1 and PHF2 partners, which co-participate to CEeRNA expression and thus to the engagement of myoblast cells into differentiation
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Gerber, Anthony Nicholas. "MyoD induces chromatin remodeling : implications for lineage determination and tumorigenesis /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6342.

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Books on the topic "My3D"

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Mynd adra'n droednoeth. Caernarfon: Gwasg y Bwthyn, 2014.

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Mynd dan groen. Llandysul: Gomer, 2010.

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Stephen, Cartwright, ed. Mynd i'r ysbyty. Caerdydd: Dref Wen, 2003.

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Jones, Wil Porthmadog. Mynd a dŵad. Dinbych, Clwyd: Gee, 1987.

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Davies, Helen Emanuel. Mynd i'r sioe! Aberystwyth: Y Ganolfan Astudiaethau Addysg, 2000.

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Griffiths, Maisie. Sami'n mynd i'r syrcas. Bangor: Canolfan Astudiaethau Iaith, 1993.

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Jones, Wil. Mynd a d^wad. Dinbych: Gwasg Gee, 1987.

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Elfyn, Menna. Mynd lawr i'r nefoedd. Llandysul: Gwasg Gomer, 1986.

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Andrew, Moira. Elliw'n mynd am dro. Caerdydd: Camfa, 1997.

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Davies, Elgan Philip. Mynd ar ôl tri. Aberystwyth: Cymdeithas Lyfrau Ceredigion, 1995.

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Book chapters on the topic "My3D"

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Sadlack, Erin A. "Marrying Where “my mynd is”." In The French Queen's Letters, 91–117. New York: Palgrave Macmillan US, 2011. http://dx.doi.org/10.1057/9780230118560_4.

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Tapscott, Stephen J., Robert L. Davis, Andrew B. Lassar, and Harold Weintraub. "MyoD: A Regulatory Gene of Skeletal Myogenesis." In Myoblast Transfer Therapy, 3–6. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_1.

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Chen, Jingjuan, Chao Wang, and Shihuan Kuang. "Transdifferentiation of Muscle Satellite Cells to Adipose Cells Using CRISPR/Cas9-Mediated Targeting of MyoD." In Methods in Molecular Biology, 25–41. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8897-6_3.

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Rudnicki, Michael A., Thomas Braun, Hans-Henning Arnold, and Rudolf Jaenisch. "Targeted Inactivation of the Muscle Regulatory Genes Myf-5 and MyoD: Effect on Muscle and Skeletal Development." In Transgenic Animals as Model Systems for Human Diseases, 143–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_9.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "MyoD." In The Gene Knockout FactsBook, 780–81. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50432-4.

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"MyoD." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1314. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_11108.

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"MYND." In Encyclopedia of Signaling Molecules, 3298. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102459.

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"MyoD." In Encyclopedia of Cancer, 2440. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3942.

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"MyD-1." In Encyclopedia of Signaling Molecules, 3279. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102447.

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"SET and MYND Domain-Containing Proteins." In Encyclopedia of Signaling Molecules, 4913. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103479.

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Conference papers on the topic "My3D"

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Hohmann, Matthias R., Michelle Hackl, Brian Wirth, Talha Zaman, Raffi Enficiaud, Moritz Grosse-Wentrup, and Bernhard Schölkopf. "MYND." In CHI '19: CHI Conference on Human Factors in Computing Systems. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3290607.3313002.

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Hohmann, Matthias R., Lisa Konieczny, Michelle Hackl, Brian Wirth, Talha Zaman, Raffi Enficiaud, Moritz Grosse-Wentrup, and Bernhard Schölkopf. "MYND." In UIST '20: The 33rd Annual ACM Symposium on User Interface Software and Technology. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3379337.3415844.

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Hecker, L., R. Jagirdar, and VJ Thannickal. "Regulation of Myofibroblast Plasticity by MyoD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1973.

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Zahavi, M., J. Zahavi, N. M. Bornstein, and A. D. Korczyn. "ENHANCED PLATELT RELEASE REACTION, INCREASED PLATELET AGGREGATION (PA) AND PLATELET THROMBOXANE B2 (TXB2) GENERATION IN MYOTONIC DYSTROPHY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644572.

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Plasma β-thromboglobulin (βTG) level, 14C 5-hydroxytryptamine (5Ht) release, PA induced by 1-epinephrine (0.2-1.0 μM) and ADP (0.5, 1.0 and 1.5 μM), and platelet TXB2 generation and eTG release after stimulation with the 2 PA inducers, was studied in platelet rich plasma of 16 patients with myotonic dystrophy (MYD) and 14 apparently healthy controls. Plasma βTG values were higher (p< 0.011) and 5Ht release was increased (p<0.035) in the patients than controls. The extent of PA induced by 1-epinephrine at 1 and 3 min. or by ADP at 3 min. was significantly raised in the MYD patients. These results indicate that the platelet α2 receptor activity as well as the release reaction is increased in MYD patients. Platelet TXB2 generation and βTG release after stimulation with ADP 1.5 μM or 1-epinephrine 1 μM were significantly more pronounced in the patients than controls (p<0.01). Furtheremore, the increased TXB2 generation correlated positively with the extent of PA induced by ADP (r=0.829 and p<0.05) or 1-epinephrine (r=0.929 and p<0.01) (Spearman one tailed test). There was no such correlation in the healthy controls. These results suggest that the enhanced PA in the MYD patients is presumably mediated through the increased platelet TXB2 synthesis. The enhanced platelet function and Ca++ TXB2 synthesis in MYD patients might be due to an increase in Ca++ uptake related to a generalized membrane abnormality.Further studies of this model inclu�jng assessment of platelet α2 receptor activity and changes in Ca++ ion fluxes through the platelet membrane, may lead to a better understanding of the basic cellular abnormalities in MYD.
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Rusli, Mohd Ezanee, Salman Yussof, Mohammad Ali, and Ahmed Abdullah Abobakr Hassan. "MySD: A Smart Social Distancing Monitoring System." In 2020 8th International Conference on Information Technology and Multimedia (ICIMU). IEEE, 2020. http://dx.doi.org/10.1109/icimu49871.2020.9243569.

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Hecker, Louise, Rajesh Jagirdar, Toni Jin, and Victor Thannickal. "MYOD Mediates The Reversible Differentiation Of Myofibroblasts." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3470.

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Narendula, Rammohan, Thanasis G. Papaioannou, and Karl Aberer. "My3: A highly-available P2P-based online social network." In 2011 IEEE International Conference on Peer-to-Peer Computing (P2P). IEEE, 2011. http://dx.doi.org/10.1109/p2p.2011.6038730.

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Levene, M. J., D. A. Dombeck, K. A. Kasischke, R. P. Molloy, R. M. Williams, W. R. Zipfel, and W. W. Webb. "GRIN lenses for deep in vivo multiphoton imaging." In Frontiers in Optics. Washington, D.C.: OSA, 2003. http://dx.doi.org/10.1364/fio.2003.my3.

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Pomella, Silvia, Prethish Sreenivas, Berkley E. Gryder, Long Wang, Matteo Cassandri, Kunal Baxi, Nicole R. Hensch, et al. "Abstract B35: Liaison between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in fusion-negative rhabdomyosarcoma." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-b35.

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Dey, Joyoti, Stephen J. Tapscott, and James M. Olson. "Abstract 1431: A novel tumor-suppressor role of MyoD, a muscle differentiation factor, in mouse models of medulloblastoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1431.

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